Basal cell carcinoma (BCC)

Basal Cell Carcinoma (BCC)
BCC is the most common cancer in humans.
Caused by UVR; PTCH gene mutation in most cases.
Clinically different types: nodular, ulcerating, pigmented, sclerosing , and superficial.

BCC is locally invasive, aggressive, and destructive but slow growing, and there is very limited (literally no) tendency to metastasize.

Skin Lesions: There are five clinical types:
1- Nodular
2- Ulcerating
3- Sclerosing (Cicatricial),
4- Superficial,
5- Pigmented.

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Basal Cell
Carcinoma (BCC)

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Basal Cell Carcinoma (BCC)
•BCCis the most common cancer in
humans.
•Caused by UVR; PTCH gene mutation in
most cases.
•Clinically different types: nodular,
ulcerating, pigmented, sclerosing , and
superficial.
The PTCH1 gene provides instructions for producing the patched-1 protein, which functions as a receptor. Receptor
proteins have specific sites into which certain other proteins, called ligands, fit like keys into locks. A protein called Sonic
Hedgehog is the ligand for the patched-1 receptor. Together, ligands and their receptors trigger signals that affect cell
development and function.Patched-1 and Sonic Hedgehog function in a pathway that is essential for early development.
This pathway plays a role in cell growth, cell specialization, and determining the shape (patterning) of many different parts
of the developing body. When Sonic Hedgehog is not present, patched-1 prevents cells from growing and dividing
(proliferating). When Sonic Hedgehog is attached, patched-1 stops suppressing cell proliferation. Based on its role in
preventing cells from proliferating in an uncontrolled way, PTCH1 is called a tumor suppressor gene.

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•BCCis locallyinvasive, aggressive, and
destructivebut slowgrowing, and there is
very limited(literally no) tendency to
metastasize.
•Treatmentis by surgical excision, Mohs
micrographic surgery, electrodesiccation,
and curettage. Also cryosurgery and
imiquimod cream.

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Epidemiology
•Age of Onset :
Older than 40 years.
•Sex :
Males > females.
•IncidenceUnited States: 500–1000 per
100,000, higher in the sunbelt; >400,000
new patients annually.
•Race: Rare in brown-and black-skinned
persons.

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Etiology
•UVR, mostly of the UVB spectrum (290–320 nm)
that induces mutations in suppressor genes. The
propensity for multiple BCC may be inherited.
Associated with mutationsin the PTCH gene in
many cases.

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Predisposing Factors
Skin phototypesI and II and albinosare
highly susceptible to develop BCC with
prolonged sun exposure.
Also a history of heavy sun exposure in
youth predisposes the skin to the
development of BCC later in life.
Previous therapy with x-rays for facial
acne greatly increases the risk of BCC

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Predisposing Factors
Superficial multicentric BCC occurs 30–40
years after ingestion of arsenic but also
without apparent cause.

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Clinical Manifestation
•Slowly evolving, usually asymptomatic.
Erosionor bleedingwith minimal trauma
may be first symptom.
•Skin Lesions: There are five clinical types:
1-Nodular
2-Ulcerating
3-Sclerosing(Cicatricial),
4-Superficial,
5-Pigmented.

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1-Nodular BCC:
•Papuleor nodule, translucent or “pearly.”
Skin-colored or reddish, smooth surface
with telangiectasia, well defined, firm.
•Portions of nodular BCC may have
erosions or stipples of melanin
pigmentation.

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Basal cell carcinoma: nodular type

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Basal cell carcinoma: nodular type
•A. A glistening, smooth plaque on the lower eyelid with
multiple telangiectasias.
•B. An oval, pearly nodule on the nose close to the inner
canthus.

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•A smooth, pearly tumor with telangiectasia below the lower
eyelid. Tumor feels hard, is well defined, and is
asymptomatic.
•A large, firm reddish glistening nodule with small ulcerations
on the nose.

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2-Ulcerating BCC:
•Ulcer (often covered with a crust) with a rolled
border (rodent ulcer), which again is translucent,
pearly, smooth with telangiectasia, and firm

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•C. Rodent ulcer in the preauricular region. A rolled pearly border
surrounds an ulcer with yellow necroses and a tiny black crust.
•D. A deep ulcer with a surrounding rolled border, smooth, glistening
and partly covered with crusts in the mandibular region. All these
lesions are hard upon palpation.

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3-Sclerosing BCC:
•Appears as a small patch of morphea or a
superficial scar, often illdefined, skin-
colored, whitish but also with peppery
pigmentation

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3-Sclerosing BCC: cont..
•Sclerosing BCC can progress to nodular
or ulcerating BCC
Basal cell carcinoma, sclerosing,
nodular, and ulcerating A large lesion,
which looks like morphea and is
whitish and firm upon palpation
but within the level of the skin, is
found on the temple and in the
supraciliar region.

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4-Superficial multicentric BCCs:
•Appear as thin plaques

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•Superficial basal cell carcinoma, invasive There are two irregular
red areas with rolled borders and central telangiectasia. In the larger
lesion the BCC is elevated with an irregular surface and now
assumes the morphology and growth behavior of a nodular BCC, on
the right the lesion is erosive and will progress to an ulcer.

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5-Pigmented BCC:
•May be brown to blue or black

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Distribution:
•Isolated single lesion; multiple lesions are
not infrequent; > 90% occur in the face.
Search carefully for “danger sites”: medial
and lateral canthi.nasolabialfold,behind
the ears . Superficial multicentricBCCs
occur on the trunk.
•BCC usually arises only from epidermis
that has a capacity to develop (hair)
follicles.

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Distribution:
Basal cell carcinoma:
predilection sites Dots
indicate
superficial multicentric
BCCs.

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Laboratory Examination
•Dermatopathology : Solid tumor consisting of
proliferating atypical basal cells, large, oval,
deep-blue staining on H&E, but with little
anaplasia and infrequent mitoses; palisading
arrangement at periphery; variable amounts of
mucinous stroma.

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Management
•Excision with primary closure, skin flaps,
or grafts. Cryosurgery and electrosurgery
are options, but only for very small lesions
and not in the danger sites or on the scalp

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Course And Prognosis
•BCC does not metastasize. The reason for this is the tumor's growth
dependency on its stroma, which on invasion of tumor cells into the
vessels is not disseminated with the tumor cells. When tumor cells
lodge at distant sites, they do not multiply and grow because of the
absence of growth factors derived from their stroma. Exceptions
occur when a BCC shows signs of dedifferentiation, for instance,
after inadequate radiotherapy. Most lesions are readily controlled by
various surgical techniques. Serious problems, however, may occur
with BCC arising in the danger sites of the head. In these sites the
tumor may invade deeply, cause extensive destruction of muscle
and bone, and even invade to the dura mater. In such cases, death
may result from hemorrhage of eroded large vessels or infection.

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•SOURCE: From FITZPATRICK’S COLOR ATLAS
AND SYNOPSIS OF CLINICAL DERMATOLOGY
SIXTH EDITION

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